The Experts below are selected from a list of 2070 Experts worldwide ranked by ideXlab platform
Claudio Ronco - One of the best experts on this subject based on the ideXlab platform.
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Cardiorenal Syndrome Type 5: In Vitro Cytotoxicity Effects on Renal Tubular Cells and Inflammatory Profile
2020Co-Authors: Alessandra Brocca, Claudio Ronco, Grazia Maria Virzi, Massimo De Cal, Stefano Marcante, Silvia Pastori, Chiara Pasqualin, Academic Editor: José A Sánchez-alcázarAbstract:Background. Cardiorenal Syndrome Type 5 (CRS Type 5) reflects concomitant cardiac and renal dysfunctions in the setting of a wide spectrum of systemic disorders. Our aim was to study in vitro effects of CRS Type 5 plasma on renal tubular cells (RTCs), in terms of cellular death and the characterization of inflammatory plasma profile in these patients. Material and Methods. We enrolled 11 CRS Type 5 patients from ICU and 16 healthy controls. Plasma from patients and controls was incubated with renal tubular cells (RTCs) and cell death was evaluated. Plasma cytokines were detected. Results. RTCs incubated with CRS Type 5 plasma showed significantly higher apoptosis and necrosis with respect to controls. Plasma cytokine profile of CRS Type 5 patients was significantly different from controls: we observed the production of pro-and anti-inflammatory mediators in these patients. Caspase-3, caspase-8, and caspase-9 were activated in cells treated with CRS Type 5 plasma compared to controls. Conclusions. Our results underline the cytotoxic effect of CRS Type 5 mediators on RTC viability, probably due to the activation of both intrinsic and extrinsic pathways of apoptosis and to the deregulation of cytokine release. The consequence may be the damage of distant organs which lead to the worsening of condition of patients
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lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in Cardiorenal Syndrome type 1
Journal of Nephrology, 2019Co-Authors: Grazia Maria Virzi, Massimo De Cal, Annalisa Angelini, Chiara Castellani, Giorgio Vescovo, Andrea Breglia, Ghada Ankawi, Chiara Bolin, Vito Cianci, Claudio RoncoAbstract:Background Cardiorenal Syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury. In this study, we evaluate the role of lipopolysaccharide (LPS) and various inflammatory markers in the developing acute kidney injury (AKI) in acute heart failure (AHF) patients.
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Cardiorenal Syndrome in acute kidney injury
Seminars in Nephrology, 2019Co-Authors: Luca Di Lullo, Antonio Bellasi, Patrick Bronson Reeves, Claudio RoncoAbstract:Varying degrees of cardiac and kidney dysfunction commonly are observed in hospitalized patients. As a demonstration of the significant interplay between the heart and kidneys, dysfunction or injury of one organ often contributes to dysfunction or injury of the other. The term Cardiorenal Syndrome (CRS) was proposed to describe this complex organ cross-talk. Type 3 CRS, also known as acute renocardiac Syndrome, is a subtype of CRS that occurs when acute kidney injury contributes to or precipitates the development of acute cardiac dysfunction. Acute kidney injury may directly or indirectly produce acute cardiac dysfunction by way of volume overload, metabolic acidosis, electrolyte disorders such as hyperkalemia and hypocalcemia, and other mechanisms. In this review, we examine the definition, epidemiology, pathophysiology, and treatment options for CRS with an emphasis on type 3 CRS.
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customization of peritoneal dialysis in Cardiorenal Syndrome by optimization of sodium extraction
CardioRenal Medicine, 2019Co-Authors: Amir Kazory, Abhilash Koratala, Claudio RoncoAbstract:Background Peritoneal dialysis (PD) has emerged as a mechanistically relevant therapeutic option for patients with heart failure (HF), volume overload, and varying degrees of renal dysfunction (i.e., chronic Cardiorenal Syndrome). Congestion has been identified as a potent ominous prognostic factor in this patient population, outperforming a number of established risk factors. As such, excess fluid removal is recognized as a relevant therapeutic target in this setting. Methods Accumulating evidence points to the importance of sodium removal as part of any decongestive strategy because extraction of sodium-free water has little or no impact on the outcomes of these patients. Hence, optimization of sodium removal by PD should be the primary focus in the setting of HF and Cardiorenal Syndrome, especially if PD is started when the patient still has adequate residual renal function for clearance of waste products. Results Herein, we provide an overview of approaches that can tailor PD treatment to the patients' characteristics and clinical needs (e.g., choice of PD modality) to fully exploit its decongestive properties. Other methods that could prove helpful in the future will also be briefly discussed. Conclusion While these strategies could help with efficient sodium extraction and volume optimization, future studies are needed to evaluate their impact on the outcomes of this specific patient population.
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Cardiorenal Syndrome an overview
Advances in Chronic Kidney Disease, 2018Co-Authors: Claudio Ronco, Antonio Bellasi, Luca Di LulloAbstract:It is well established that a large number of patients with acute decompensated heart failure present with various degrees of heart and kidney dysfunction usually primary disease of heart or kidney often involve dysfunction or injury to the other. The term Cardiorenal Syndrome increasingly had been used without a consistent or well-accepted definition. To include the vast array of interrelated derangements and to stress the bidirectional nature of heart-kidney interactions, a new classification of the Cardiorenal Syndrome with 5 subtypes that reflect the pathophysiology, the time frame, and the nature of concomitant cardiac and renal dysfunction was proposed. Cardiorenal Syndrome can generally be defined as a pathophysiological disorder of the heart and kidneys, in which acute or chronic dysfunction of one organ may induce acute or chronic dysfunction to the other. Although Cardiorenal Syndrome was usually referred to as acute kidney dysfunction following acute cardiac disease, it is now clearly established that impaired kidney function can have an adverse impact on cardiac function.
Grazia Maria Virzi - One of the best experts on this subject based on the ideXlab platform.
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Cardiorenal Syndrome Type 5: In Vitro Cytotoxicity Effects on Renal Tubular Cells and Inflammatory Profile
2020Co-Authors: Alessandra Brocca, Claudio Ronco, Grazia Maria Virzi, Massimo De Cal, Stefano Marcante, Silvia Pastori, Chiara Pasqualin, Academic Editor: José A Sánchez-alcázarAbstract:Background. Cardiorenal Syndrome Type 5 (CRS Type 5) reflects concomitant cardiac and renal dysfunctions in the setting of a wide spectrum of systemic disorders. Our aim was to study in vitro effects of CRS Type 5 plasma on renal tubular cells (RTCs), in terms of cellular death and the characterization of inflammatory plasma profile in these patients. Material and Methods. We enrolled 11 CRS Type 5 patients from ICU and 16 healthy controls. Plasma from patients and controls was incubated with renal tubular cells (RTCs) and cell death was evaluated. Plasma cytokines were detected. Results. RTCs incubated with CRS Type 5 plasma showed significantly higher apoptosis and necrosis with respect to controls. Plasma cytokine profile of CRS Type 5 patients was significantly different from controls: we observed the production of pro-and anti-inflammatory mediators in these patients. Caspase-3, caspase-8, and caspase-9 were activated in cells treated with CRS Type 5 plasma compared to controls. Conclusions. Our results underline the cytotoxic effect of CRS Type 5 mediators on RTC viability, probably due to the activation of both intrinsic and extrinsic pathways of apoptosis and to the deregulation of cytokine release. The consequence may be the damage of distant organs which lead to the worsening of condition of patients
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lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in Cardiorenal Syndrome type 1
Journal of Nephrology, 2019Co-Authors: Grazia Maria Virzi, Massimo De Cal, Annalisa Angelini, Chiara Castellani, Giorgio Vescovo, Andrea Breglia, Ghada Ankawi, Chiara Bolin, Vito Cianci, Claudio RoncoAbstract:Background Cardiorenal Syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury. In this study, we evaluate the role of lipopolysaccharide (LPS) and various inflammatory markers in the developing acute kidney injury (AKI) in acute heart failure (AHF) patients.
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Cardiorenal Syndrome type 4 from chronic kidney disease to cardiovascular impairment
European Journal of Internal Medicine, 2016Co-Authors: Antonio Granata, Claudio Ronco, Grazia Maria Virzi, Massimo De Cal, Anna Clementi, Alessandra Brocca, V R Scarfia, Luca Zanoli, Salvatore Corrao, Lorenzo MalatinoAbstract:Cardiorenal Syndrome type 4 (CRS type 4), or chronic renocardiac Syndrome, has been defined as "chronic abnormalities in renal function leading to cardiac disease" and recognizes the extreme burden of cardiovascular disease (CVD) risk in patients with chronic kidney disease (CKD). CKD is common and increasingly recognized as a risk factor for CVD. Even though the treatment for CVD has dramatically improved over the past decades, it still takes responsibility for up to 50% of deaths in CKD patients. For this reason, patients with CKD should be thoroughly evaluated for cardiovascular risk factors that require careful management, given the significant burden of CRS type 4 on the healthcare system. This review focuses on the most significant conventional and non-conventional CVD risk factors related to CKD.
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Cardiorenal Syndrome type 5 in sepsis role of endotoxin in cell death pathways and inflammation
Kidney & Blood Pressure Research, 2016Co-Authors: Grazia Maria Virzi, Massimo De Cal, Anna Clementi, Alessandra Brocca, Stefano Marcante, Claudio RoncoAbstract:Background/Aims: Cardiorenal Syndrome Type 5 (CRS Type 5) is characterized by concomitant cardiac and renal dysfunction in the setting of different systemic disor
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the role of congestion in Cardiorenal Syndrome type 2 new pathophysiological insights into an experimental model of heart failure
CardioRenal Medicine, 2016Co-Authors: Annalisa Angelini, Claudio Ronco, Grazia Maria Virzi, Chiara Castellani, Marny Fedrigo, Gaetano Thiene, Marialuisa Valente, Giorgio VescovoAbstract:Background: In Cardiorenal Syndrome type 2 (CRS2), the role of systemic congestion in heart failure (HF) is still obscure. We studied a model of CRS2 [monocrotali
Massimo De Cal - One of the best experts on this subject based on the ideXlab platform.
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Cardiorenal Syndrome Type 5: In Vitro Cytotoxicity Effects on Renal Tubular Cells and Inflammatory Profile
2020Co-Authors: Alessandra Brocca, Claudio Ronco, Grazia Maria Virzi, Massimo De Cal, Stefano Marcante, Silvia Pastori, Chiara Pasqualin, Academic Editor: José A Sánchez-alcázarAbstract:Background. Cardiorenal Syndrome Type 5 (CRS Type 5) reflects concomitant cardiac and renal dysfunctions in the setting of a wide spectrum of systemic disorders. Our aim was to study in vitro effects of CRS Type 5 plasma on renal tubular cells (RTCs), in terms of cellular death and the characterization of inflammatory plasma profile in these patients. Material and Methods. We enrolled 11 CRS Type 5 patients from ICU and 16 healthy controls. Plasma from patients and controls was incubated with renal tubular cells (RTCs) and cell death was evaluated. Plasma cytokines were detected. Results. RTCs incubated with CRS Type 5 plasma showed significantly higher apoptosis and necrosis with respect to controls. Plasma cytokine profile of CRS Type 5 patients was significantly different from controls: we observed the production of pro-and anti-inflammatory mediators in these patients. Caspase-3, caspase-8, and caspase-9 were activated in cells treated with CRS Type 5 plasma compared to controls. Conclusions. Our results underline the cytotoxic effect of CRS Type 5 mediators on RTC viability, probably due to the activation of both intrinsic and extrinsic pathways of apoptosis and to the deregulation of cytokine release. The consequence may be the damage of distant organs which lead to the worsening of condition of patients
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lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in Cardiorenal Syndrome type 1
Journal of Nephrology, 2019Co-Authors: Grazia Maria Virzi, Massimo De Cal, Annalisa Angelini, Chiara Castellani, Giorgio Vescovo, Andrea Breglia, Ghada Ankawi, Chiara Bolin, Vito Cianci, Claudio RoncoAbstract:Background Cardiorenal Syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury. In this study, we evaluate the role of lipopolysaccharide (LPS) and various inflammatory markers in the developing acute kidney injury (AKI) in acute heart failure (AHF) patients.
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Cardiorenal Syndrome type 4 from chronic kidney disease to cardiovascular impairment
European Journal of Internal Medicine, 2016Co-Authors: Antonio Granata, Claudio Ronco, Grazia Maria Virzi, Massimo De Cal, Anna Clementi, Alessandra Brocca, V R Scarfia, Luca Zanoli, Salvatore Corrao, Lorenzo MalatinoAbstract:Cardiorenal Syndrome type 4 (CRS type 4), or chronic renocardiac Syndrome, has been defined as "chronic abnormalities in renal function leading to cardiac disease" and recognizes the extreme burden of cardiovascular disease (CVD) risk in patients with chronic kidney disease (CKD). CKD is common and increasingly recognized as a risk factor for CVD. Even though the treatment for CVD has dramatically improved over the past decades, it still takes responsibility for up to 50% of deaths in CKD patients. For this reason, patients with CKD should be thoroughly evaluated for cardiovascular risk factors that require careful management, given the significant burden of CRS type 4 on the healthcare system. This review focuses on the most significant conventional and non-conventional CVD risk factors related to CKD.
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Cardiorenal Syndrome type 5 in sepsis role of endotoxin in cell death pathways and inflammation
Kidney & Blood Pressure Research, 2016Co-Authors: Grazia Maria Virzi, Massimo De Cal, Anna Clementi, Alessandra Brocca, Stefano Marcante, Claudio RoncoAbstract:Background/Aims: Cardiorenal Syndrome Type 5 (CRS Type 5) is characterized by concomitant cardiac and renal dysfunction in the setting of different systemic disor
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oxidative stress dual pathway induction in Cardiorenal Syndrome type 1 pathogenesis
Oxidative Medicine and Cellular Longevity, 2015Co-Authors: Grazia Maria Virzi, Massimo De Cal, Anna Clementi, Alessandra Brocca, Giorgio Vescovo, Chiara Bolin, Sonya Day, Silvia Pastori, Claudio RoncoAbstract:Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (P < 0.05). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.
Andrew R Kompa - One of the best experts on this subject based on the ideXlab platform.
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Cardiorenal Syndrome multi organ dysfunction involving the heart kidney and vasculature
British Journal of Pharmacology, 2020Co-Authors: Andrew R Kompa, Darren J Kelly, Feby Savira, Ruth Magaye, Danny Liew, C ReidAbstract:Cardiorenal Syndrome (CRS) is a multi-organ disease, encompassing heart, kidney and vascular system dysfunction. CRS is a worldwide problem, with high morbidity, mortality, and inflicts a significant burden on the health care system. The pathophysiology is complex, involving interactions between neurohormones, inflammatory processes, oxidative stress and metabolic derangements. Therapies remain inadequate, mainly comprising symptomatic care with minimal prospect of full recovery. Challenges include limiting the contradictory effects of multi-organ targeted drug prescriptions and continuous monitoring of volume overload. Novel strategies such as multi-organ transplantation and innovative dialysis modalities have been considered but lack evidence in the CRS context. The adjunct use of pharmaceuticals targeting alternative pathways showing positive results in preclinical models also warrants further validation in the clinic. In recent years, studies have identified the involvement of gut dysbiosis, uraemic toxin accumulation, sphingolipid imbalance and other unconventional contributors, which has encouraged a shift in the paradigm of CRS therapy.
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protein bound uremic toxins a long overlooked culprit in Cardiorenal Syndrome
American Journal of Physiology-renal Physiology, 2016Co-Authors: Suree Lekawanvijit, Andrew R Kompa, Henry KrumAbstract:Protein-bound uremic toxins (PBUTs) accumulate once renal excretory function declines and are not cleared by dialysis. There is increasing evidence that PBUTs exert toxic effects on many vital organs, including the kidney, blood vessels, and heart. It has been suggested that PBUTs are likely to be a potential missing link in Cardiorenal Syndrome, based on the high incidence of cardiovascular events and mortality in the dialysis population, which are dramatically reduced in successful kidney transplant recipients. These data have led the call for more effective dialysis or additional adjunctive therapy to eradicate these toxins and their adverse biological effects. Indoxyl sulfate and p-cresyl sulfate are the two most problematic PBUTs, conferring renal and cardiovascular toxicity, and are derived from dietary amino acid metabolites by colonic microbial organisms. Therefore, targeting the colon where these toxins are initially produced appears to be a potential therapeutic alternative for patients with chronic kidney disease. This strategy, if approved, is likely to be applicable to predialysis patients, thereby potentially preventing progression of chronic kidney disease to end-stage renal disease as well as preventing the development of Cardiorenal Syndrome.
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Cardiorenal Syndrome the emerging role of protein bound uremic toxins
Circulation Research, 2012Co-Authors: Suree Lekawanvijit, Andrew R Kompa, Bing H Wang, Darren J Kelly, Henry KrumAbstract:Cardiorenal Syndrome is a condition in which a complex interrelationship between cardiac dysfunction and renal dysfunction exists. Despite advances in treatment of both cardiovascular and kidney disease, Cardiorenal Syndrome remains a major global health problem. Characteristic of the pathophysiology of Cardiorenal Syndrome is bidirectional cross-talk; mediators/substances activated by the disease state of 1 organ can play a role in worsening dysfunction of the other by exerting their biologically harmful effects, leading to the progression of the Syndrome. Accumulation of uremic toxins is a hallmark of renal excretory dysfunction. Removal of some toxins by conventional dialysis is particularly problematic because of their high protein binding. In this review, we demonstrate that protein-bound uremic toxins may play an important role in progression of cardiovascular disease in the setting of chronic kidney disease. The highly protein-bound uremic toxin indoxyl sulfate has emerged as a potent toxin adversely affecting both the kidney and heart. Direct cardiac effects of this toxin have been recently demonstrated both in vitro and in vivo. Specifically, potent fibrogenic and prohypertrophic effects, as well as oxidative stress-inducing effects, appear to play a central role in both renal and cardiac pathology. Many of these adverse effects can be suppressed by use of a gut adsorbent, AST-120. Potential mechanisms underlying indoxyl sulfate-induced Cardiorenal fibrosis are discussed. Future research and clinical implications conclude this review.
Michael P Hutchens - One of the best experts on this subject based on the ideXlab platform.
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the acute kidney injury to chronic kidney disease transition in a mouse model of acute Cardiorenal Syndrome emphasizes the role of inflammation
Kidney International, 2020Co-Authors: Katsuyuki Matsushita, Turgay Saritas, Mahaba B Eiwaz, Nicholas Mcclellan, Ian Coe, Wenbin Zhu, Mohammed Z Ferdaus, Lynn Y Sakai, James A Mccormick, Michael P HutchensAbstract:Acute Cardiorenal Syndrome is a common complication of acute cardiovascular disease. Studies of acute kidney injury (AKI) to chronic kidney disease (CKD) transition, including patients suffering acute cardiovascular disease, report high rates of CKD development. Therefore, acute Cardiorenal Syndrome associates with CKD, but no study has established causation. To define this we used a murine cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) model or sham procedure on male mice. CA was induced with potassium chloride while CPR consisted of chest compressions and epinephrine eight minutes later. Two weeks after AKI was induced by CA/CPR, the measured glomerular filtration rate (GFR) was not different from sham. However, after seven weeks the mice developed CKD, recapitulating clinical observations. One day, and one, two, and seven weeks after CA/CPR, the GFR was measured, and renal tissue sections were evaluated for various indices of injury and inflammation. One day after CA/CPR, acute Cardiorenal Syndrome was indicated by a significant reduction of the mean GFR (649 in sham, vs. 25 μL/min/100g in CA/CPR animals), KIM-1 positive tubules, and acute tubular necrosis. Renal inflammation developed, with F4/80 positive and CD3-positive cells infiltrating the kidney one day and one week after CA/CPR, respectively. Although there was functional recovery with normalization of GFR two weeks after CA/CPR, deposition of tubulointerstitial matrix proteins α-smooth muscle actin and fibrillin-1 progressed, along with a significantly reduced mean GFR (623 in sham vs. 409 μL/min/100g in CA/CPR animals), proteinuria, increased tissue transforming growth factor-β, and fibrosis establishing the development of CKD seven weeks after CA/CPR. Thus, murine CA/CPR, a model of acute Cardiorenal Syndrome, causes an AKI-CKD transition likely due to prolonged renal inflammation.
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determination of renal function and injury using near infrared fluorimetry in experimental Cardiorenal Syndrome
American Journal of Physiology-renal Physiology, 2017Co-Authors: Mizuko Ikeda, Rumie Wakasaki, Katie J Schenning, Thomas Swide, Jeong Heon Lee, Bernie M Miller, Hak Soo Choi, Sharon Anderson, Michael P HutchensAbstract:Cardiorenal Syndrome type 1 causes acute kidney injury but is poorly understood; animal models and diagnostic aids are lacking. Robust noninvasive measurements of glomerular filtration rate are req...